Vascular complications of chronic hyperglycemia including diabetic retinopathy are an increasing therapeutic and socioeconomic challenge. The epidemiology of diabetic eye disease has been well described, and there is as yet no clear indication for a reduction of incidence of blindness. Due to the complex multifactorial nature of the damage to diabetic vessels, it had been difficult to identify key targets for treatment and prevention. Novel techniques to study molecules and mechanisms involved in retinal vessel development and vascular cell interactions improved the understanding of retinal cell biology and pathobiology. A unifying concept has been proposed which links hyperglycemia-induced mitochondrial overproduction of reactive oxygen species with long-known biochemical alterations such as the formation of advanced glycation end products or the activation of the protein kinase C pathway. Specific inhibitors were identified that inhibited multiple biochemical abnormalities downstream of oxidative stress induced by high glucose.
Copyright (c) 2007 S. Karger AG, Basel